Research Topic: The role of the G-actin sequestering peptide Thymosin β-4 in renal podocyte health and disease. Qualifications: 2017 - Biomedical Science BSc (Hons), University of Kent Scholarships: University of Kent Vice Chancellor's Research Scholarship
Chronic Kidney Disease (CKD) is a devastating condition that affects more than 1.8 million people in the United Kingdom. Despite current treatments, a significant proportion of patients progresses to end stage renal failure which requires lifelong dialysis or transplantation, underlining the urgent need for new therapies. During CKD, the kidney gradually becomes unable to sufficiently filter the blood. One of the main cells responsible for the ultrafiltration are podocytes which are comprised of a cell body extending many projections, called foot processes, wrapping around the capillaries in the glomerulus. These processes interdigitate with each other forming a critical component of the filtration barrier. The actin cytoskeleton is responsible for maintaining the structure of the foot processes and during disease, the actin cytoskeleton becomes disorganised and foot processes lose their specialised shape and structure. Thymosin -4 (TB4) is the main G-actin sequestering peptide in cells with a critical role in maintaining the actin cytoskeleton. Previous studies from our group have shown that loss of TB4 in podocytes exacerbates kidney disease and disrupts the actin cytoskeleton of the podocytes. My research is focused on the therapeutic potential of exogenous TB4 on injured podocytes in vitro and in vivo. We hypothesise that TB4 will be able to protect kidney function by preventing the cytoskeletal rearrangements in podocytes.
Supervisors: Dr Elisavet Vasilopoulou, Professor Claire Peppiatt-Wildman and Dr David Long (UCL) Research Group: Biological Sciences
Conference Activities: Oral/Keynote Presentations: 1. Mason W, Peppiatt-Wildman C, Long DA, Vasilopoulou E. Exogenous thymosin β-4 protects kidney function by modulating the rearrangement of the podocyte cytoskeleton. Nephrogenesis workshop. 2. Mason W, Peppiatt-Wildman C, Long DA, Vasilopoulou E. Exogenous thymosin β-4 protects kidney function by modulating the rearrangement of the podocyte cytoskeleton. UCL Renal Tripartite meeting. November 2019, London, U.K. June 2019, London, U.K. Poster Presentations: 1. Mason W, Peppiatt-Wildman C, Long DA, Vasilopoulou E. The role of the actin-sequestering protein, thymosin b-4, on renal podocyte function. Europhysiology. September 2018, London, U.K. 2.Mason W, Peppiatt-Wildman C, Long DA, Vasilopoulou E. The role of the actin-sequestering protein, thymosin b-4, on renal podocyte function. U.K. Kidney Week. June 2019, Brighton, U.K. Outreach events: 1. NIHR Great Ormand Street Hospital BRC Family Fun Day, October 2019.